Memory specific responses have historically been restricted to adaptive T and B cells; however, natural killer (NK) cells, part of the innate immune arm, are a prime example of cells that can cross this innate-adaptive border in a context-dependent manner. During mouse cytomegalovirus (MCMV) infection, a subset of NK cells can undergo clonal-like expansion and generate long lived progeny that can mediate a robust secondary response, similar to the adaptive immune system. Previous work demonstrated that these antigen-specific NK cells displayed a core epigenetic signature like that of antigen-specific CD8+T cells. Notably, AP-1 factor motifs were enriched among regions that became more accessible, with the AP-1 transcription factor JunB seen to be highly expressed in both NK cells and CD8+T cells throughout infection. To investigate the role of JunB in NK and CD8+ T cells, JunB was genetically depleted in mice using a Cre-lox system. During MCMV infection, deletion of JunB in NK cells and CD8+ T cells at the beginning of the infection resulted in defective effector and memory cell formation. This phenomenon seems to be specific to infection as no significant difference in homeostatic proliferation was observed between WT and JunB deficient NK and CD8+ T cells. We observed no difference in IFNy production in JunB deficient stimulated NK cells, but showed alterations in proliferative capacity and potentially survival. By tracking JunB dependent differentially accessible regions established by published data, we found that early JunB activity in CD8+T cells contributes to establishing the later memory landscape. Overall, we implicate JunB as a critical component of memory formation during infection.